Neurological complications are common in AIDS and with the expected increase in cases in the decade, the neurological disease must be of great concern. To devise appropriate strategies to prevent moderation and that of the AIDS dementia complex, we propose fundamental studies of pathogenesis. We will take advantage of our previous experience in a related lentivirus disease in sheep, visna, and our expertise with in situ hybridization technology to (1) define unambiguously the types of cells in AIDS dementia which harbor the causative agent (HIV); (2) evaluate the changes in the expression of macrophage genes such as IL-1 which might play a role in tissue damage; (3) differentially screen cDNA libraries to identify genes whose expression changes in concent with vacuolation, the most prominent pathological manifestation of the AIDS neurological disease.